ライフサイエンスコーパス: SVR

1 SVR at 12 weeks (SVR12) was assessed in the modified ful

2 SVR is a relevant clinical end point, but further analys

3 SVR rates in HIV/HCV GT1-coinfected patients were high.

4 SVR reduced the risk of HCC.

5 SVR was achieved by 60.5% of patients (52.9% with HCV ge

6 SVR was achieved in 28 of the 29 patients (97%).

7 SVR was associated with a decreased incidence of hepatoc

8 SVR was not associated with significant changes in BMD n

9 SVR was similar between African Americans (90.5% [546/60

10 ed individuals were included if they met: 1) SVR with DAA-based combination; 2) Liver stiffness (LS)

11 -acting antivirals, which resulted in a 100% SVR rate in era 3 and a decrease in the number of patien

12 s in men with HIV infections, reports a 100% SVR.

13 without RBV for 12 or 24 weeks produced 100% SVR 12 in patients with HCV recurrence after liver trans

14 iagnosis of HCC, 140 no SVR patients and 397 SVR patients were diagnosed with incident HCC.

15 1735 nmol/L) was common (50% active HCV, 43% SVR) and did not different between groups.

16 ately 1.6 years, 195 no SVR patients and 598 SVR patients died.

17 Overall, 1,067 patients did not achieve SVR (no SVR) and 13,992 patients achieved SVR.

18 ent HCC rates than those who did not achieve SVR.

19 riple therapy could be sufficient to achieve SVR in patients with undetectable viremia at week 1, but

20 e use of RBV may not be necessary to achieve SVR in this patient population.

21 ication of treatment and capacity to achieve SVR.

22 patients with advanced fibrosis, who achieve SVR with DAA, HIV-coinfection seems to be associated wit

23 tment in clinical trials and did not achieve SVRs were enrolled in a long-term registry (#NCT01457768

24 virologic response (SVR), and 8.0% achieved SVR.

25 f 497 patients treated for HCV, 257 achieved SVR and had at least 1 subsequent RNA measurement.

26 f 58.2 months, 668 patients (50.5%) achieved SVR.

27 Eighty-two patients (82%) achieved SVR, which was not associated with baseline OAT status (

28 patients, and 395 patients (95.9%) achieved SVR at 12 weeks: 96.6%, 94.5%, and 90.9% among LT, KT, a

29 ), and 70 (94.6% of DAA completers) achieved SVR.

30 notype 5a without cirrhosis who had achieved SVR at post-treatment week 4 relapsed at post-treatment

31 compared with participants who had achieved SVR, whereas FT did not differ.

32 chronic hepatitis C virus who have achieved SVR.

33 llowing criteria were included: (i) Achieved SVR with DAA-including regimen; (ii) LS >= 9.5 kPa befor

34 ollowing criteria were included: i) Achieved SVR with DAA-including regimen; ii) LS >=9.5 kPa before

35 Forty-one achieved SVR(12) , 10 had undetectable viral loads but are not el

36 Three patients achieved SVR(12) , 1 has completed DAA therapy, and 2 remain on t

37 Six patients achieved SVR(12) and 1 patient remains on treatment.

38 516 patients achieved SVR, a response rate of 86% (95% CI, 83.0% to 88.7%), wi

39 ve SVR (no SVR) and 13,992 patients achieved SVR.

40 57.6% UMHS and 52.0% PUHSC patients achieved SVR.

41 compensated advanced fibrosis that achieved SVR after direct antivirals.

42 Those who achieved SVR (n=141; 94%) were eligible for this extension study.

43 for recurrent hepatitis C virus who achieved SVR after reLT compared with those who did not (P = 0.03

44 anges in LDL among CHC patients who achieved SVR differed by IFNL4 genotype, which implicates the int

45 ompensation in patients with PH who achieved SVR to IFN-free therapy.

46 t differed between participants who achieved SVR vs those who relapsed was ribavirin concentration at

47 epatitis C virus (HCV) patients who achieved SVR with DAAs from 129 Veterans Health Administration ho

48 and B cells in 20 HCV patients who achieved SVR with Sofosbuvir and Ledipasvir for 12 weeks and comp

49 Of 141 who achieved SVR, 114 had a least 1 visit in the extension study (62%

50 Of 141 who achieved SVR, 114 had a least one visit in the extension study (6

51 500 lifetime cost, compared to 22% achieving SVR, with 5.49 QALYs and a $161 300 lifetime cost, with

52 were associated with high rates of achieving SVR, compared to standard care.

53 All patients achieving SVR after HCV treatment were followed with HCV RNA measu

54 In addition, subjects achieving SVR had increasing expression of the transcription facto

55 Conclusion: Those achieving SVR after direct-acting antiviral treatment had signific

56 py was more impressive among those achieving SVR.

57 PPI use with LDV/SOF +/- RBV did not affect SVR (89.7% [131/146] with PPI and 91.5% [613/670] withou

58 sent in 13 patients at baseline and 25 after SVR, although only 3 patients had increased pulmonary re

59 of noninvasive markers and its changes after SVR.

60 re associated with persistence of CSPH after SVR.

61 LSMs can rule out the presence of CSPH after SVR.

62 ith a very low risk of HCC development after SVR.

63 those who report ongoing risk factors after SVR.

64 ad the highest annual incidence of HCC after SVR (1.82 vs 0.34/100 person-years in patients without c

65 Reassessment of HVPG after SVR improved prognostication in patients with pretreatme

66 Systemic hemodynamics improved after SVR.

67 ctive HCV coinfection, but information after SVR is lacking.

68 ctive HCV coinfection, but information after SVR is lacking.

69 kPa before treatment to 18 (14-28) kPa after SVR (P < .05).

70 h a reduction in LSM to below 13.6 kPa after SVR still had CSPH.

71 Low FT persisted after SVR (pre-treatment 58%, post-SVR 54%, P = .72).

72 IV had smaller transaminase reductions after SVR.

73 (HCC) - or requiring liver transplant after SVR.

74 ma (HCC)-or requiring liver transplant after SVR.

75 eased from 3.8%/year in the first year after SVR to 2.4%/year by the fourth year (P=.01).

76 rate (per 1000 PYFU) in the first year after SVR was highest in those who reported high-frequency IDU

77 ar); risk remained high for many years after SVR.

78 remained above 2%/year, even 10 years after SVR.

79 An SVR after antiviral therapy was associated with decrease

80 An SVR after antiviral therapy was associated with improved

81 Patients who did not achieve an SVR after treatment experienced worsening HRQL scores in

82 A total of 200 patients achieved an SVR (22.4%) (94 patients with HCV infection, 98 patients

83 ncluded in the CirVir cohort who achieved an SVR.

84 SVR) and an association between achieving an SVR and improved clinical outcomes.

85 chieving favorable Baveno VI status after an SVR was associated with the absence of PHT progression.

86 Patients with cirrhosis before an SVR to treatment for HCV infection continue to have a hi

87 We found an SVR to reduce overall mortality and risk of death from l

88 Lack of an SVR and grade 1 EV were independently associated with pr

89 ted cirrhosis and to study the effects of an SVR on the progression of PHT.

90 ion; there are also data to indicate that an SVR can reduce mortality.

91 7 locus was significantly associated with an SVR.

92 19.2 (95% CI 17.4-21.1) for those without an SVR (P < .0001).

93 ratio [HR] compared with patients without an SVR, 0.29; 95% confidence interval [CI], 0.19-0.43; P <

94 In the per-protocol analysis, SVR rate achieved was 98.2% (29,090/29,620), and 78.1% (

95 In multivariable Cox regression analysis, SVR was associated with a reduction in HCC risk (HR, 95%

96 (hazard ratio [HR] 0.53, 95% CI .46-.63) and SVR (HR 0.81, 95% CI .70-.93) were associated with a sig

97 Secondary: HCV treatment completion and SVR 12 weeks after treatment completion.

98 g the algorithms with the DAA initiation and SVR results from the registry.

99 rtal hypertension (CSPH; HVPG >=10 mmHg) and SVR after DAA therapy showed that disappearance of CSPH

100 were predictors of HCC while study site and SVR were not.

101 Favorable Baveno VI status and SVR were independently associated with survival.

102 on sBMD for the interaction between time and SVR either in the LS (P=0.801) or the FN (P=0.911).

103 =0.123) for the interaction between time and SVR.

104 valuating population-level DAA treatment and SVR outcomes.

105 icipants through HCV care and treatment, and SVR rates demonstrate the real-world ability of achievin

106 None out of 374 patients with LS <14kPa at SVR time-point developed a liver complication or require

107 None of the 374 patients with LS <14kPa at SVR time-point developed a liver complication or require

108 herapy and; iii) LS measurement available at SVR.

109 erapy; and (iii) LS measurement available at SVR.

110 ores (1.37 [1.03-1.82]), CPT class B or C at SVR (10.71 [1.32-87.01]), CD4 cell counts <200/uL at SVR

111 ores (1.37 [1.03-1.82]), CPT class B or C at SVR (10.71 [1.32-87.01]), CD4 cell counts <200/uL at SVR

112 me-point (4.42 [1.49-13.15]), FIB-4 index at SVR (1.39 [1.13-1.70]) and LS at SVR (1.05 [1.02-1.08] f

113 me-point (4.42 [1.49-13.15]), FIB-4 index at SVR (1.39 [1.13-1.70]), and LS at SVR (1.05 [1.02-1.08]

114 4 index at SVR (1.39 [1.13-1.70]), and LS at SVR (1.05 [1.02-1.08] for 1 kPa increase).

115 -4 index at SVR (1.39 [1.13-1.70]) and LS at SVR (1.05 [1.02-1.08] for 1 kPa increase).

116 d to analyze the predictive ability of LS at SVR for liver complications in HIV/HCV-coinfected patien

117 d to analyze the predictive ability of LS at SVR for liver complications in people living with HIV/HC

118 [sHR=7.9 (2.5-24.9); p<0.001], MELD score at SVR>10 [sHR=1.37 (1.01-1.86); p=0.043] and LS value at S

119 71 [1.32-87.01]), CD4 cell counts <200/uL at SVR time-point (4.42 [1.49-13.15]), FIB-4 index at SVR (

120 71 [1.32-87.01]), CD4 cell counts <200/uL at SVR time-point (4.42 [1.49-13.15]), FIB-4 index at SVR (

121 R=1.37 (1.01-1.86); p=0.043] and LS value at SVR [sHR=1.03 (1.01-1.06) for 1 kPa increase; p=0.011].

122 otic, 91% were genotype 3 and 91.9% attained SVR.

123 hen IST and VVS, with diverse changes in CO, SVR, and central blood volume.

124 clinical characteristics, and comorbidities, SVR was independently associated with reduced risk of de

125 Among patients treated with DAA, SVR was associated with a considerable reduction in the

126 less, CSPH persists in most patients despite SVR, indicating persistent risk of decompensation.

127 t start and/or end dates, 314 had documented SVR.

128 Following SVR, mean change in HbA1c was -0.022 +/- 0.53%; however,

129 e investigated hemodynamic changes following SVR in patients with CSPH and whether liver stiffness me

130 pendent predictors of change in FT following SVR.

131 Despite improvements in SHBG following SVR, low FT was common and persisted after HCV clearance

132 idence of 8.9 per 1000 person-years: 6.9 for SVR and 21.6 for NSVR per 1000 person-years.

133 Overall 37,256 persons were eligible for SVR assessment, of these only 29,620 (79.5%) returned fo

134 Overall, 37 256 persons were eligible for SVR assessment; of these, only 29 620 (79.5%) returned f

135 ectable viral loads but are not eligible for SVR(12) , and 7 remain on treatment.

136 ation of therapy was a predictive factor for SVR, while poor hematological tolerance of ribavirin req

137 255), to identify the predictive factors for SVR, and to evaluate the impact of HEV RNA mutations on

138 atients and 2.6 deaths/100 patient years for SVR patients, a 78.9% reduction (P < 0.001).

139 patients and 1.9 HCCs/100 patient years for SVR patients, an 83.5% reduction (P < 0.001).

140 Four SVR algorithms relied on fulfilling treatment algorithm

141 virus-associated cirrhosis and CSPH who had SVR to interferon-free therapy at 6 Liver Units in Spain

142 ir, and sofosbuvir/velpatasvir achieved high SVR rates with good safety profile, comparable to those

143 red to PWID in OAT programs resulted in high SVR, despite ongoing drug use.

144 Direct-acting antivirals produce high SVR rates in white, black, Hispanic, and Asian/Pacific I

145 ment groups and could not reproduce the high SVR rates observed.

146 hereas Asian race was associated with higher SVR rates compared to white patients.

147 Viral load did not impact SVR rates in cohort B.

148 tions (95%, P = .174), with no difference in SVR between those who did and did not miss 7 consecutive

149 lations (95%, P=0.174) with no difference in SVR between those who did and did not miss at least seve

150 n of ribavirin was associated with increased SVR rates for certain DAA regimens and patient groups.

151 he impact of direct-acting antiviral-induced SVR on all-cause mortality and on incident hepatocellula

152 A DAA-induced SVR reduces a patient's risk of cirrhosis and hepatocell

153 Ribavirin did not influence SVR rates and was more often used in those with higher B

154 lant recipients; ribavirin did not influence SVR, and graft rejection was rare.

155 ild-Turcotte-Pugh class C disease, had lower SVR rates (78% to 87%) than other populations.

156 rapy, black patients had significantly lower SVR than white patients when treated for 8 weeks but not

157 DV/SOF +/- RBV was not associated with lower SVR rates, but cirrhosis was.

158 nts without a prior diagnosis of HCC, 140 no SVR patients and 397 SVR patients were diagnosed with in

159 up period of approximately 1.6 years, 195 no SVR patients and 598 SVR patients died.

160 ates were 11.5 HCCs/100 patient years for no SVR patients and 1.9 HCCs/100 patient years for SVR pati

161 deaths/100 patient years of follow-up for no SVR patients and 2.6 deaths/100 patient years for SVR pa

162 rall, 1,067 patients did not achieve SVR (no SVR) and 13,992 patients achieved SVR.

163 ed with reduced risk of death compared to no SVR (hazard ratio, 0.26; 95% confidence interval, 0.22-0

164 ooled HR, 0.29 [95% CI, 0.23 to 0.38]) vs no SVR.

165 improved clinical outcomes compared with no SVR.

166 We found that to predict observed SVR rates it was necessary to assume that ledipasvir, GS

167 many more studies supporting the benefits of SVR and DAA therapies, including a decline in patients a

168 change in risk behavior, and determinants of SVR.

169 Likewise, no significant effect of SVR was observed in plasma levels of sRANKL (P=0.205), O

170 No significant effect of SVR was observed on sBMD for the interaction between tim

171 Primary outcomes were effects of SVR on the hepatic, pulmonary, and systemic hemodynamics

172 At week 24, the primary endpoint of SVR of 35% or more was achieved by 42 (19%) patients in

173 dipasvir-sofosbuvir provided a high level of SVR in those without cirrhosis.

174 0.02) was the only independent predictor of SVR in HCV non-genotype 1 patients.

175 DHCR7 rs12785878 GT/TT had a higher rate of SVR than those with the GG allele (59.7% vs. 43.4%, P =

176 otype 3 who had cirrhosis, compared rates of SVR in both groups with a performance goal of 83%.

177 eks, but the 2 regimens had similar rates of SVR in patients with HCV genotype 3 and cirrhosis.

178 th HCV treatment can result in high rates of SVR while reducing risks associated with drug use.

179 ificant difference regarding pooled rates of SVR, adherence, and discontinuation between patients on

180 LS at the time of SVR after DAA therapy predicts the clinical outcome of H

181 LS at the time of SVR after DAA therapy predicts the clinical outcome of p

182 Methods based on SVR seem to be suboptimal to handle sparse data and yiel

183 Overall SVR rates were 89.8% (95% confidence interval [CI] 89.2-

184 Overall SVR was 94% (CI, 89% to 97%); the SVR rate was 98% in th

185 In 4 additional participants, SVR was achieved but the participants were viremic at la

186 Similarly, the pooled SVR was 88% (95% CI, 80% to 93%) in PWID and the pooled

187 Among patients on OST, the pooled SVR was 90% (95% confidence interval [CI], 87% to 93%) a

188 1) found DAA regimens associated with pooled SVR rates greater than 95% across genotypes, and low sho

189 B-4 scores from >=3.25 pre-SVR to <3.25 post-SVR was associated with an approximately 50% lower risk

190 nce, especially if FIB-4 remains >=3.25 post-SVR.

191 persisted after SVR (pre-treatment 58%, post-SVR 54%, P = .72).

192 scores >=3.25 (HCC risk 1.22%/year) and post-SVR FIB-4 scores >=3.25 (HCC risk 2.39%/year); risk rema

193 sed during treatment, then decreased at post-SVR year 1; however, in patients with TT/TT, genotype di

194 but then it decreased to 97.7 mg/dL by post-SVR year 1 (P < .001 compared with DAA; P = .0013 compar

195 (P < .0001) while FT remained unchanged post-SVR.

196 ly mean ALT continued to decrease until post-SVR.

197 available to guide clinicians on which post-SVR patients should be monitored vs discharged, how to m

198 A decrease in FIB-4 scores from >=3.25 pre-SVR to <3.25 post-SVR was associated with an approximate

199 a low risk of HCC, except for those with pre-SVR FIB-4 scores >=3.25 (HCC risk 1.22%/year) and post-S

200 eatment with DAAs (n = 9784), those with pre-SVR fibrosis-4 (FIB-4) scores >=3.25 had a higher annual

201 present before treatment initiation predict SVR and eventual development of a higher frequency of fu

202 rhosis, and hepatic decompensation predicted SVR at 12 weeks.

203 cell proliferation before therapy predicted SVR and was associated with the magnitude of the HCV-spe

204 Cirrhosis was predictive of reduced SVR (0.51 [95% confidence interval {CI}, .31-.87]; P = .

205 ed on the support vector machine regression (SVR) algorithm to solve the key gap between the need for

206 s: those based on support vector regression (SVR) and those based on binary classification.

207 we use a trained support vector regression (SVR) model to select best configurations.

208 the HARPE data by support vector regression (SVR) to provide comprehensive models for the sequence mo

209 cinoma (HCC) after sustained viral response (SVR) and need lifelong surveillance.

210 improved with HCV sustained viral response (SVR) in coinfection.

211 e the effects of a sustained viral response (SVR) on outcomes of patients with hepatitis C virus (HCV

212 patients achieved sustained viral response (SVR) within the first year after reLT in each subsequent

213 uld ever achieve a sustained viral response (SVR), with 7.21 QALYs and a $245 500 lifetime cost, comp

214 d, 592 (36%) had a sustained viral response (SVR).

215 patients achieved sustained viral response (SVR).

216 e who achieved sustained virologic response (SVR) (n = 141; 94%) were eligible for this extension stu

217 a 90% rate of sustained virologic response (SVR) 4 weeks after treatment, a second cohort receiving

218 Sustained virologic response (SVR) after direct acting antiviral agents (DAAs) holds p

219 r those with a sustained virologic response (SVR) and 19.2 (95% CI 17.4-21.1) for those without an SV

220 likelihood of sustained virologic response (SVR) and an association between achieving an SVR and imp

221 Rates of sustained virologic response (SVR) at 12 weeks were available on 412 patients, and 395

222 predictors of sustained virologic response (SVR) at 24 weeks following discontinuation of therapy we

223 adherence and sustained virologic response (SVR) have not been evaluated in the direct-acting antivi

224 and achieved a sustained virologic response (SVR) in the Veterans Health Administration (29,033 treat

225 convinced that sustained virologic response (SVR) is a validated surrogate outcome and that direct-ac

226 HIV) in whom a sustained virologic response (SVR) is achieved.

227 d, historical, sustained virologic response (SVR) of 60% with pegylated-interferon/ribavirin.

228 The impact of sustained virologic response (SVR) on mortality after direct-acting antiviral treatmen

229 ns showed high sustained virologic response (SVR) rates (>95%) in patients with HCV genotype 1 infect

230 High sustained virologic response (SVR) rates have been observed after 6 weeks of anti-HCV

231 changes after sustained virologic response (SVR) remain unknown.

232 Sustained virologic response (SVR) to interferon (IFN)-free therapies ameliorates port

233 lower rates of sustained virologic response (SVR) to interferon-based treatments for chronic hepatiti

234 leted therapy, sustained virologic response (SVR) was achieved in 43 (89.6%).

235 Sustained virologic response (SVR) was not achieved in 9 participants: 7 had follow-up

236 attainment of sustained virologic response (SVR) were associated with significantly lower mortality

237 e assessed for sustained virologic response (SVR), and 8.0% achieved SVR.

238 end point was sustained virologic response (SVR), and secondary end points included uptake of and re

239 cted to assess sustained virologic response (SVR), discontinuation rates, adherence, and HCV reinfect

240 high rates of sustained virologic response (SVR), generally exceeding 90%.

241 not differ by sustained virologic response (SVR), HIV, diabetes, or fibrosis.

242 e in achieving sustained virologic response (SVR), however, whether successful DAA treatment reconsti

243 a DAA-induced sustained virologic response (SVR).

244 treatment, and sustained virologic response (SVR).

245 ment and after sustained virologic response (SVR).

246 9.4%) achieved sustained virologic response (SVR).

247 nitiators) had sustained virologic response (SVR).

248 could predict sustained virologic response (SVR).

249 nfection after sustained virologic response (SVR).

250 4%) achieved a sustained virologic response (SVR).

251 0%) achieved sustained virological response (SVR) 12.

252 atients with sustained-virological response (SVR) at 12 and/or 24 weeks post-treatment.

253 outcome was sustained virological response (SVR) at 12 weeks after completion of direct-acting antiv

254 s (HCV) with sustained virological response (SVR) develop hepatic complications.

255 atients with sustained virological response (SVR) develops hepatic complications.

256 o assess the sustained virological response (SVR) in a large cohort of solid organ transplant (SOT) r

257 Sustained virological response (SVR) is a non-validated surrogate outcome.

258 ients with a sustained virological response (SVR) or nonsustained virological response (NSVR).

259 te achieving sustained virological response (SVR) to therapy, remain at risk of liver decompensation.

260 who achieve sustained virological response (SVR) with direct-acting antiviral (DAA).

261 (HCC) after sustained virological response (SVR) with direct-acting antivirals (DAA) is unclear.

262 n achieved a sustained virological response (SVR) with glecaprevir/pibrentasvir, with no virological

263 e, we report sustained virological response (SVR), safety data, health-related quality-of-life (HRQOL

264 reatment and sustained virological response (SVR).

265 gical response sustain virological response (SVR)12 was 91.8% and 86% of cohorts A and B, respectivel

266 5 treated with sustained virologic response [SVR], 43 during treatment, and 281 treated without SVR),

267 d not achieve sustained virologic responses (SVRs) after treatment with direct-acting antivirals.

268 Our results demonstrate that SVR with DAA therapy is effective in the reconstitution

269 The SVR rate was 98.2% (29 090/29 620) in the per-protocol a

270 Overall SVR was 94% (CI, 89% to 97%); the SVR rate was 98% in the DOT group, 94% in the GT group,

271 vious to treatment; 3) LS measurement at the SVR time-point.

272 in HCV non-genotype 1-infected patients, the SVR rate did not differ between the two groups (63.3% an

273 After a first course of ribavirin, the SVR rate was 81.2%.

274 The experimental results showed that the SVR model can accurately and effectively predict blood p

275 for the sequence motifs, and found that the SVR-based approach is more effective than a consensus-ba

276 rOD for 12 (n = 9) or 24 (n = 36) weeks; the SVR rate at 12 weeks was 93%.

277 herence decreased over the course of therapy SVR was high in non-adherent (89%) and adherent populati

278 on of direct-acting antiviral (DAA) therapy (SVR(12) ).

279 IU/mL) 12 weeks after the end of treatment (SVR) or an undetectable level of HBV DNA.

280 gs, but among those who completed treatment, SVR was achieved at a high rate.

281 Hepatitis C virus SVR decreased monocyte interferon genes MX1, IFI27, and

282 and 21 completed HCV treatment (n = 16 with SVR and n = 5 without).

283 r cocaine use was negatively associated with SVR in univariate analysis, but this association was not

284 lable, but DAA regimens were associated with SVR rates greater than 5% and few short-term harms relat

285 lth treatment at intake were associated with SVR.

286 1 compared with DAA; P = .0013 compared with SVR).

287 l/L) was more prevalent in participants with SVR compared with active HCV (P = .002); however, low FT

288 endpoint was the proportion of patients with SVR at 12 weeks after treatment (SVR12).

289 Patients with SVR may still have a risk of HCC and need to be regularl

290 The associated risk of HCC in patients with SVR was 0.37 (0.22-0.63) for those without cirrhosis and

291 Among the 18,076 patients with SVR, 544 incident cases of HCC were diagnosed during the

292 Among patients with SVR, advanced age, male gender, cirrhosis, decreased pla

293 However, in patients with SVR, the absolute risk of HCC remained high in patients

294 cases of HCC, including 183 in patients with SVR.

295 eated participants without SVR vs those with SVR had a higher risk of liver events (IRR, 6.79 [95% CI

296 In those with SVR, interferon-inducible protein 10, ATX, and Mac2BP le

297 he evidence for the benefits associated with SVRs in different clinical settings and challenges to da

298 difference between patients with and without SVR.

299 ve individuals, treated participants without SVR vs those with SVR had a higher risk of liver events

300 43 during treatment, and 281 treated without SVR), and 2503 HCV-seronegative controls.